English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Rheumatoid arthritis-associated joint pain is frequently observed independentof disease activity, suggesting unidentified pain mechanisms. We demonstratethat antibodies binding to cartilage, specific for collagen type II (CII) orcartilage oligomeric matrix protein (COMP), elicit mechanical hypersensitivityin mice, uncoupled from visual, histological and molecular indications ofinflammation. Cartilage antibody-induced pain-like behavior does not depend oncomplement activation or joint inflammation, but instead on tissue antigenrecognition and local immune complex (IC) formation. smFISH and IHC suggestthat neuronal Fcgr1 and Fcgr2b mRNA are transported to peripheral ends ofprimary afferents. CII-ICs directly activate cultured WT but not FcR{\gamma}chain-deficient DRG neurons. In line with this observation, CII-IC does notinduce mechanical hypersensitivity in FcR{\gamma} chain-deficient mice.Furthermore, injection of CII antibodies does not generate pain-like behaviorin FcR{\gamma} chain-deficient mice or mice lacking activating Fc{\gamma}Rs inneurons. In summary, this study defines functional coupling betweenautoantibodies and pain transmission that may facilitate the development of newdisease-relevant pain therapeutics.

Cartilage-binding antibodies induce pain through immune complex-mediated activation of neurons